DIETARY OLIGOFRUCTOSE MODIFIES THE IMPACT OF FRUCTOSE ON HEPATIC TRIACYLGLYCEROL METABOLISM

The aim was to investigate if chronic feeding with oligofructose (OFS) , a nondigestible fructan that decreases triacylglycerol-very-low-dens ity lipoproteins (TAG-VLDLs) in the serum of rats by reducing hepatic de novo lipogenesis, could counteract the impact of fructose on TAG me tabolism. Male Wistar rats fed a standard diet supplemented or not wit h 10% OFS for 30 days received either tap water or a 10% fructose drin king solution for 48 hours. TAG, phospholipids (PLs), cholesterol, and free fatty acids were assayed both in serum and in liver. Fatty acid de novo synthesis, esterification, and beta-oxidation were assessed in the liver by measuring the activity of key enzymes: fatty acid syntha se (FAS), phosphatidate phosphohydrolase (PAP), glycerol-3-phosphate a cyltransferase (GPAT), and carnitine palmitoyltransferase-I (CPT-I), r espectively. The acute load of fructose increased (1) both liver and s erum TAG without affecting other lipids, and (2) de novo fatty acid sy nthesis and esterification, through induction of FAS and PAP without a ffecting CPT-L. Long-term feeding with OFS protected rats against live r TAG accumulation induced by fructose. The lower lipogenic capacity o f the liver could be the key event in this protection, since even afte r the fructose load FAS activity remained significantly lower in OFS-f ed rats. However, despite its protective effect on the liver, OFS was not able to prevent fructose-induced hypertriglyceridemia, suggesting that OFS feeding could not counteract the fructose-induced defect in T AG-VLDL clearance. Copyright (C) 1996 by W.B. Saunders Company